A PI3Kγ signal regulates macrophage recruitment to injured tissue for regenerative cell survival
The interaction between immune cells and injured tissues is crucial for regeneration. Previous studies have shown that macrophages attenuate inflammation caused by injuries to support the survival of primed regenerative cells. Macrophage loss in zebrafish mutants like cloche (clo) causes extensive a...
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| Veröffentlicht in: | Development, growth & differentiation growth & differentiation, 2022-10, Vol.64 (8), p.433-445 |
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| creator | Zhou, Siyu Liu, Zhengcheng Kawakami, Atsushi |
| description | The interaction between immune cells and injured tissues is crucial for regeneration. Previous studies have shown that macrophages attenuate inflammation caused by injuries to support the survival of primed regenerative cells. Macrophage loss in zebrafish mutants like cloche (clo) causes extensive apoptosis in the regenerative cells of the amputated larval fin fold. However, the mechanism of interaction between macrophage and injured tissue is poorly understood. Here, we show that a phosphoinositide 3‐kinase gamma (PI3Kγ)‐mediated signal is essential for recruiting macrophages to the injured tissue. PI3Kγ inhibition by the PI3Kγ‐specific inhibitor, 5‐quinoxalin‐6‐ylmethylene‐thiazolidine‐2,4‐dione (AS605240 or AS), displayed a similar apoptosis phenotype with that observed in clo mutants. We further show that PI3Kγ function during the early regenerative stage is necessary for macrophage recruitment to the injured site. Additionally, protein kinase B (Akt) overexpression in the AS‐treated larvae suggested that Akt is not the direct downstream mediator of PI3Kγ for macrophage recruitment, while it independently plays a role for the survival of regenerative cells. Together, our study reveals that PI3Kγ plays a role for recruiting macrophages in response to regeneration. |
| doi_str_mv | 10.1111/dgd.12809 |
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Previous studies have shown that macrophages attenuate inflammation caused by injuries to support the survival of primed regenerative cells. Macrophage loss in zebrafish mutants like cloche (clo) causes extensive apoptosis in the regenerative cells of the amputated larval fin fold. However, the mechanism of interaction between macrophage and injured tissue is poorly understood. Here, we show that a phosphoinositide 3‐kinase gamma (PI3Kγ)‐mediated signal is essential for recruiting macrophages to the injured tissue. PI3Kγ inhibition by the PI3Kγ‐specific inhibitor, 5‐quinoxalin‐6‐ylmethylene‐thiazolidine‐2,4‐dione (AS605240 or AS), displayed a similar apoptosis phenotype with that observed in clo mutants. We further show that PI3Kγ function during the early regenerative stage is necessary for macrophage recruitment to the injured site. Additionally, protein kinase B (Akt) overexpression in the AS‐treated larvae suggested that Akt is not the direct downstream mediator of PI3Kγ for macrophage recruitment, while it independently plays a role for the survival of regenerative cells. Together, our study reveals that PI3Kγ plays a role for recruiting macrophages in response to regeneration.</description><identifier>ISSN: 0012-1592</identifier><identifier>EISSN: 1440-169X</identifier><identifier>DOI: 10.1111/dgd.12809</identifier><identifier>PMID: 36101496</identifier><language>eng</language><publisher>Japan: Wiley Subscription Services, Inc</publisher><subject>AKT protein ; Animals ; Apoptosis ; Cell Survival ; Kinases ; macrophage ; Macrophages ; Macrophages - metabolism ; Mutants ; Phenotypes ; Phosphatidylinositol 3-Kinase ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphoinositide-3 Kinase Inhibitors ; PI3K ; Proto-Oncogene Proteins c-akt - metabolism ; Recruitment ; regeneration ; zebrafish ; Zebrafish - metabolism</subject><ispartof>Development, growth & differentiation, 2022-10, Vol.64 (8), p.433-445</ispartof><rights>2022 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Society of Developmental Biologists.</rights><rights>2022 The Authors. Development, Growth & Differentiation published by John Wiley & Sons Australia, Ltd on behalf of Japanese Society of Developmental Biologists.</rights><rights>2022. This article is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4719-70a0f551a4c2c00d233c2b0a86511f9cb7800805853a7ddc1319c1b0bd3b833b3</cites><orcidid>0000-0001-9461-6372</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdgd.12809$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdgd.12809$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,1416,1432,27922,27923,45572,45573,46407,46831</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36101496$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Siyu</creatorcontrib><creatorcontrib>Liu, Zhengcheng</creatorcontrib><creatorcontrib>Kawakami, Atsushi</creatorcontrib><title>A PI3Kγ signal regulates macrophage recruitment to injured tissue for regenerative cell survival</title><title>Development, growth & differentiation</title><addtitle>Dev Growth Differ</addtitle><description>The interaction between immune cells and injured tissues is crucial for regeneration. Previous studies have shown that macrophages attenuate inflammation caused by injuries to support the survival of primed regenerative cells. Macrophage loss in zebrafish mutants like cloche (clo) causes extensive apoptosis in the regenerative cells of the amputated larval fin fold. However, the mechanism of interaction between macrophage and injured tissue is poorly understood. Here, we show that a phosphoinositide 3‐kinase gamma (PI3Kγ)‐mediated signal is essential for recruiting macrophages to the injured tissue. PI3Kγ inhibition by the PI3Kγ‐specific inhibitor, 5‐quinoxalin‐6‐ylmethylene‐thiazolidine‐2,4‐dione (AS605240 or AS), displayed a similar apoptosis phenotype with that observed in clo mutants. We further show that PI3Kγ function during the early regenerative stage is necessary for macrophage recruitment to the injured site. 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Together, our study reveals that PI3Kγ plays a role for recruiting macrophages in response to regeneration.</description><subject>AKT protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell Survival</subject><subject>Kinases</subject><subject>macrophage</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Mutants</subject><subject>Phenotypes</subject><subject>Phosphatidylinositol 3-Kinase</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphoinositide-3 Kinase Inhibitors</subject><subject>PI3K</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Recruitment</subject><subject>regeneration</subject><subject>zebrafish</subject><subject>Zebrafish - metabolism</subject><issn>0012-1592</issn><issn>1440-169X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp1kc9KHTEYxYNY9NZ20RcoATd2Mfp9SeZPNoJotVLBLlroLmQymTGX-XObTG7xufoefSZze620gski8OWXw8k5hLxDOMa0TpquOUZWgdwhCxQCMizk912yAECWYS7ZPnkdwhIAhEC2R_Z5gYBCFguiz-iXa_759y8aXDfqnnrbxV7PNtBBGz-t7nRn09D46ObBjjOdJ-rGZfS2obMLIVraTn7zzI7W69mtLTW272mIfu3Wun9DXrW6D_bt43lAvl1-_Hr-Kbu5vbo-P7vJjChRZiVoaPMctTDMADSMc8Nq0FWRI7bS1GUFUEFe5VyXTWOQozRYQ93wuuK85gfkdKu7ivVgG5O8et2rlXeD9vdq0k79fzO6O9VNayUrVjDBk8DRo4CffkQbZjW4sPmKHu0Ug2IlCl5JVhYJPXyGLqfoU3wbKm2JKeBEfdhSKccQvG2fzCCoTXEqFaf-FJfY9_-6fyL_NpWAky3w0_X2_mUldXF1sZV8AGy7o3c</recordid><startdate>202210</startdate><enddate>202210</enddate><creator>Zhou, Siyu</creator><creator>Liu, Zhengcheng</creator><creator>Kawakami, Atsushi</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9461-6372</orcidid></search><sort><creationdate>202210</creationdate><title>A PI3Kγ signal regulates macrophage recruitment to injured tissue for regenerative cell survival</title><author>Zhou, Siyu ; Liu, Zhengcheng ; Kawakami, Atsushi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4719-70a0f551a4c2c00d233c2b0a86511f9cb7800805853a7ddc1319c1b0bd3b833b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>AKT protein</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell Survival</topic><topic>Kinases</topic><topic>macrophage</topic><topic>Macrophages</topic><topic>Macrophages - metabolism</topic><topic>Mutants</topic><topic>Phenotypes</topic><topic>Phosphatidylinositol 3-Kinase</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphoinositide-3 Kinase Inhibitors</topic><topic>PI3K</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Recruitment</topic><topic>regeneration</topic><topic>zebrafish</topic><topic>Zebrafish - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Siyu</creatorcontrib><creatorcontrib>Liu, Zhengcheng</creatorcontrib><creatorcontrib>Kawakami, Atsushi</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Development, growth & differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Siyu</au><au>Liu, Zhengcheng</au><au>Kawakami, Atsushi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A PI3Kγ signal regulates macrophage recruitment to injured tissue for regenerative cell survival</atitle><jtitle>Development, growth & differentiation</jtitle><addtitle>Dev Growth Differ</addtitle><date>2022-10</date><risdate>2022</risdate><volume>64</volume><issue>8</issue><spage>433</spage><epage>445</epage><pages>433-445</pages><issn>0012-1592</issn><eissn>1440-169X</eissn><abstract>The interaction between immune cells and injured tissues is crucial for regeneration. Previous studies have shown that macrophages attenuate inflammation caused by injuries to support the survival of primed regenerative cells. Macrophage loss in zebrafish mutants like cloche (clo) causes extensive apoptosis in the regenerative cells of the amputated larval fin fold. However, the mechanism of interaction between macrophage and injured tissue is poorly understood. Here, we show that a phosphoinositide 3‐kinase gamma (PI3Kγ)‐mediated signal is essential for recruiting macrophages to the injured tissue. PI3Kγ inhibition by the PI3Kγ‐specific inhibitor, 5‐quinoxalin‐6‐ylmethylene‐thiazolidine‐2,4‐dione (AS605240 or AS), displayed a similar apoptosis phenotype with that observed in clo mutants. We further show that PI3Kγ function during the early regenerative stage is necessary for macrophage recruitment to the injured site. Additionally, protein kinase B (Akt) overexpression in the AS‐treated larvae suggested that Akt is not the direct downstream mediator of PI3Kγ for macrophage recruitment, while it independently plays a role for the survival of regenerative cells. Together, our study reveals that PI3Kγ plays a role for recruiting macrophages in response to regeneration.</abstract><cop>Japan</cop><pub>Wiley Subscription Services, Inc</pub><pmid>36101496</pmid><doi>10.1111/dgd.12809</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-9461-6372</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | AKT protein Animals Apoptosis Cell Survival Kinases macrophage Macrophages Macrophages - metabolism Mutants Phenotypes Phosphatidylinositol 3-Kinase Phosphatidylinositol 3-Kinases - metabolism Phosphoinositide-3 Kinase Inhibitors PI3K Proto-Oncogene Proteins c-akt - metabolism Recruitment regeneration zebrafish Zebrafish - metabolism |
| title | A PI3Kγ signal regulates macrophage recruitment to injured tissue for regenerative cell survival |
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